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Determination of bacterial susceptibility of E.coli and S.aureus towards selected antibiotics

Institution: University of Kabianga

Course: Bachelor of Science Biochemistry

Content Category: Research Projects

Posted By: Horrizon

Document Type: DOCX

Number of Pages: 44

Price: KES 250
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Summary

Determination of bacterial susceptibility of E.coli and S.aurius towards selected Antibiotics.

CHAPTER ONE
1.0 INTRODUCTION
1.1 Background information
E. coli is part of normal flora found in the digestive system of humans and animals. However, it is the most frequent cause of hospital and community-acquired infections such as Urinary tract infections and septicemia. It is ranked among the leading causes of foodborne diseases globally. Most strains with disease-causing properties are commonly transmitted from animals to human beings through the food chain. Resistance in E.coli occurs either through a series of mutations which is associated with fluoroquinolone resistance. It is also attributed to the acquisition of mobile genetic materials which confer resistance to broad-spectrum penicillins. For example, ampicillin. Resistance to third-generation cephalosporins is attributed to enzymes known as extended-spectrum beta-lactamases (ESBLS). These enzymes can destroy the beta-lactam ring of beta-lactam antibiotics.
S. aureus is a Gram-positive bacteria that is categorized as normal flora but is a major cause of infections in humans. It is a major cause of skin infections, sepsis, and most importantly the common cause of wounds after an operation. Other strains produce toxic chemicals that sometimes cause food poisoning. The discovery of penicillin by Alexander Fleming in 1920 brought hope to the world especially to World War II soldiers in the fight against bacterial infections. The emergence of resistant strains later was known to be mediated by beta-lactamase enzymes which inactivate the beta-lactam antibiotics. MRSA is caused by a genetic mutation. These deadly strains have a gene (mecA) that codes for penicillin-binding protein and thus makes the penicillinase-stable antibiotics ineffective(Ventola, 2015).
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